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The Corticotropin-Releasing Factor Release in Rat Hypophysial Portal Blood Is Mediated by Brain Catecholamines
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1987
Year
Vnab LesionsAdrenal GlandNeuroendocrine MechanismHypothalamic PeptideNeurologyNeurochemistryHealth SciencesStress HormoneHypothalamusMedicineNeuropharmacologyNervous SystemEndocrinologyPharmacologyBrain CatecholaminesNeurophysiologyNeuroanatomyPhysiologyNeuroendocrine DisorderNeuroscienceBiological PsychiatryCentral Nervous SystemCorticotropin-releasing Factor ReleaseCrf ReleaseCrf LevelsNeuropeptides
In order to study the involvement of the hypothalamic corticotropin-releasing factor (CRF) in catecholamine-induced adrenocorticotropin (ACTH) secretion, we have measured CRF levels in rat hypophysial portal blood (HPB) after the pharmacological destruction of the ventral noradrenergic bundle (VNAB), using 6-hydroxydopamine (6-OHDA) stereotaxically injected into the VNAB. CRF levels in HPB were measured by radioimmunoassay, and the effects of 6-OHDA injection were controlled by the determination of catecholamine concentrations in the total hypothalamus. VNAB lesions induced a dramatic decrease in norepinephrine and epinephrine hypothalamic concentration. The CRF levels in HPB were also significantly reduced. These results suggest that central catecholamines exert a direct stimulatory control on the CRF release and play a major role in stress-induced ACTH secretion.